ICBII Update on the Road to the Cure - September 2022

A Real-Time Science Report
Ram S. Bhatt, PhD., Chief Science Officer

In the August 2022 Newsletter we described that in most neurodegenerative diseases, including Parkinson’s, myelin degeneration leading to axonal and neuronal dysfunction takes place long before the symptoms and alpha-synuclein clumps appear in the brain. This hypothesis is based upon Alois Alzheimer’s observation of more than 100 years ago, that neurons of Alzheimer’s patients are compromised 10–20 years before the symptoms appear. It is not to say that clearing excess oligomeric alpha-synuclein from the brain of Parkinson’s patients is not important, but any therapy should be administered at a very early stage when alpha-synuclein oligomeric species just start forming, long before the patients see their doctors for symptoms they are experiencing. Unfortunately, today we do not have a technology sensitive enough to detect very low concentrations of brain oligomeric alpha-synuclein in asymptomatic Parkinson’s patients. 

Axons and Neurons
Our central nervous system (which includes the brain and spinal cord) is made up of two basic types of cells: neurons and glial cells. Neurons are information cells that use electrical impulses and chemical signals to transmit information between different areas of the brain, and between the brain and the rest of the nervous system. Everything we think and feel and do would be impossible without the work of neurons. Glial cells support neurons. The glial cells are further divided into astrocytes and oligodendrocytes.

Neurons have three basic parts: a cell body and two extensions called an axon (see below) and a dendrite. Within the cell body is a nucleus, which controls the cell’s activities and contains the cell’s genetic material. The axon looks like a long tail and transmits messages from the cell. Dendrites look like the branches of a tree and receive messages for the cell. Neurons communicate with each other by sending chemicals, called neurotransmitters, across a tiny space, called a synapse, between the axons and dendrites of adjacent neurons. The following picture will give a pictorial view of what neuron looks like.

Upon injury, either through an accident or inflammation as in the case of Parkinson’s, the axon is damaged, and neurons become dysfunctional. The brain appears to react to an injury by over producing some proteins which thwart axon regeneration. 

ICBII Approach – We are working on inhibiting the function of proteins that interfere with axonal regeneration. We plan to target bad proteins by developing blood-brain barrier permeable SMART Molecules for these bad proteins to neutralize their negative effect on axonal regeneration. For proprietary reasons, we cannot share the names of these proteins in a newsletter but readers who are inquisitive are welcome to come to ICBII, sign an NDA so that we can openly share our entire scientific plan to discuss rejuvenation of axonal regeneration, and potentially reverse Parkinson’s disease for the benefit of millions of patients worldwide. 

Why Us? – The pharmaceutical companies have been using antibody drugs with very little brain uptake. ICBII’s SMART Molecules have shown to have 1-2 logs higher brain uptake than drugs used by big pharma. So, chances of our success in reversing Parkinson’s disease are higher than any other technology used by other companies.

ADDITIONALLY, WOULD YOU LIKE TO HELP get ICBII’s drugs to market faster? The joy of being a part of these historical events can be had by helping ICBII find the funds to bring these trials to fruition through your investing, and by finding others with the financial ability and humanitarian mindset to accomplish the, until now, impossible. Please contact ICBII directly through their website ICBII.com or by phone 858-455-9880.

IMAGINE the world without Parkinson’s, MSA, or Alzheimer’s disease.

JUST IMAGINE.